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A glycogen storage disease (GSD, also glycogenosis and dextrinosis) is a metabolic disorder caused by a deficiency of an enzyme or transport protein affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.
Hypoalbuminemia (or hypoalbuminaemia) is a medical sign in which the level of albumin in the blood is low. [1] This can be due to decreased production in the liver, increased loss in the gastrointestinal tract or kidneys, increased use in the body, or abnormal distribution between body compartments.
GSD Ia is caused by a deficiency in the enzyme glucose-6-phosphatase; GSD Ib, a deficiency in the transport protein glucose-6-phosphate translocase. Because glycogenolysis is the principal metabolic mechanism by which the liver supplies glucose to the body during fasting , both deficiencies cause severe hypoglycemia and, over time, excess ...
Most individuals with G6PD deficiency are asymptomatic.When it induces hemolysis, it is usually is short-lived. [5]Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X-chromosome in certain cells creates a population of G6PD-deficient ...
The two organs most commonly affected are the liver and the skeletal muscle. Glycogen storage diseases that affect the liver typically cause hepatomegaly and hypoglycemia; those that affect skeletal muscle cause exercise intolerance, progressive weakness and cramping. [1] Glucose-6-phosphate isomerase deficiency affects step 2 of glycolysis.
In humans, the tyrosine aminotransferase protein is encoded by the TAT gene. [7] A deficiency of the enzyme in humans can result in what is known as type II tyrosinemia, wherein there is an abundance of tyrosine as a result of tyrosine failing to undergo an aminotransferase reaction to form 4-hydroxyphenylpyruvate. [8]
All plasma proteins except Gamma-globulins are synthesised in the liver. [1] Human serum albumin, osmolyte and carrier protein; α-fetoprotein, the fetal counterpart of serum albumin; Soluble plasma fibronectin, forming a blood clot that stops bleeding; C-reactive protein, opsonin on microbes, [2] acute phase protein; Various other globulins
Pyruvate kinase deficiency is an inherited metabolic disorder of the enzyme pyruvate kinase which affects the survival of red blood cells. [ 4 ] [ 5 ] Both autosomal dominant and recessive inheritance have been observed with the disorder; classically, and more commonly, the inheritance is autosomal recessive .
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